Evidence map›Paper›PMID 30264934›Full record

ArticleCNS neuroscience & therapeutics2019

Inhibition of ferroptosis attenuates tissue damage and improves long-term outcomes after traumatic brain injury in mice.

Bao-Shu Xie, Yi-Qin Wang, Yong Lin, Qing Mao, Jun-Feng Feng, Guo-Yi Gao, Ji-Yao Jiang

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 3 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  19. PredictiveACS omega · 2026
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156 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Bao-Shu XieDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0002-0684-5341
Yi-Qin WangSino-French Research Center for Life Sciences and Genomics, State Key Laboratory of Medical Genomics, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yong LinDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Qing MaoDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jun-Feng FengDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Guo-Yi GaoDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Ji-Yao JiangDepartment of Neurosurgery, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsFerroptosis, a new form of iron-dependent programmed cell death, has been shown to be involved in a range of diseases. However, the role of ferroptosis in traumatic brain injury (TBI) has yet to be elucidated. We aimed to investigate whether ferroptosis is induced after TBI and whether the inhibition of ferroptosis would protect against traumatic brain injury in a controlled cortical impact injury (CCI) mouse model.

methodsAfter establishing the TBI model in mice, we determined the biochemical and morphological changes associated with ferroptosis, including iron accumulation with Perl's staining, neuronal cell death with Fluoro-Jade B (FJB) staining, iron metabolism dysfunction with Western blotting, reactive oxygen species (ROS) accumulation with malondialdehyde (MDA) assays, and shrunken mitochondria with transmission electron microscopy. Furthermore, a specific inhibitor of ferroptosis, ferrostatin-1(fer-1), was administrated by cerebral ventricular injection after CCI. We used cresyl violet (CV) staining to assess lesion volume, along with the Morris water maze and beam walk test to evaluate long-term outcomes.

resultsTBI was followed by iron accumulation, dysfunctional iron metabolism, the upregulation of ferroptosis-related genes, reduced glutathione peroxidase (GPx) activity, and the accumulation of lipid-reactive oxygen species (ROS). Three days (d) after TBI, transmission electron microscopy (TEM) confirmed that the mitochondria had shrunk a typical characteristic of ferroptosis. Importantly, the administration of Fer-1 by cerebral ventricular injection significantly reduced iron deposition and neuronal degeneration while attenuating injury lesions and improving long-term motor and cognitive function.

conclusionThis study demonstrated an effective method with which to treat TBI by targeting ferroptosis.

Indexed as

AnimalsBrainBrain Injuries, TraumaticCyclohexylaminesFerroptosisIronMaleMiceMice, Inbred C57BLPhenylenediaminesReactive Oxygen SpeciesTreatment OutcomeCyclohexylaminesferrostatin-1IronPhenylenediaminesReactive Oxygen Speciesferroptosisiron accumulationlipid ROS accumulationtraumatic brain injury (TBI)

Identifiers

PMID30264934
PMCPMC6488926

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.